[These results suggest that the increased expression of FasL in GD thyrocytes, the down-regulation of Fas expression by TSH or possibly by TSH receptor autoantibody, and the overexpression of Bcl-2, which could render thyrocytes resistant to FasL-mediated elimination, may thus be involved in the pathogenesis of GD.]. Sentence from MEDLINE/PubMed, a database of the U.S. National Library of Medicine.
Gene-disease associations inferred from text-mining the literature.
DisGeNET evidence - LITERATURE